Neural mechanisms by which gravitational stimuli and stress affect the secretion of renin and other hormones

The present goal is to determine by the production of discrete lesions the parts of the hypothalamus and brainstem that are involved in serotonin-mediated increases in renin secretion. A variety of stimuli which act in different ways to increase renin stimuli were developed and standardized. The experiments with p-chloroamphetamine (PCA) demonstrated that there is a serotonergic pathway which projects from the dorsal raphe nuclei to the paraventricular nuclei and the vetromedial nuclei of the hypothalamus; that projection from paraventricular nuclei to the brainstem and spinal cord may be oxytocinergic; and that the pathway from the spinal cord to the renin secreting cells is sympathetic. The demonstration that paraventicular lesions lower circulating renin substrate is important because it raises the possibility that substrate secretion is under neural control, either via the pituitary or by direct neural pathways. The discovery that lesions of the ventromedial nuclei appear to abolish the increase in renin secretion produced by many different stimuli without affecting the concentration of renin substrate in the plasma makes the position of the hypothalamus in the regulation of fluid and electrolyte balance more prominent than previously suspected.